Inhibition of mitochondrial function induces an integrated stress response in oligodendroglia

This publication has 42 references indexed in Scilit:

• Severe Impairment of Complex I–Driven Adenosine Triphosphate Synthesis in Leber Hereditary Optic Neuropathy Cybrids
  Archives of Neurology, 2005
• Mitochondrial Signaling
  Molecular Cell, 2004
• Mitochondrial dysfunction as a cause of optic neuropathies
  Progress in Retinal and Eye Research, 2004
• Loss of m-AAA protease in mitochondria causes complex I deficiency and increased sensitivity to oxidative stress in hereditary spastic paraplegia
  The Journal of cell biology, 2003
• Mitochondrial stress-induced calcium signaling, phenotypic changes and invasive behavior in human lung carcinoma A549 cells
  Oncogene, 2002
• Mitochondria: regulators of signal transduction by reactive oxygen and nitrogen species 1,2 1Guest Editor: Harry Ischiropoulos 2This article is part of a series of reviews on “Reactive Nitrogen Species, Tyrosine Nitration and Cell Signaling.” The full list of papers may be found on the homepage of the journal.
  Free Radical Biology & Medicine, 2002
• Functional Analysis of Lymphoblast and Cybrid Mitochondria Containing the 3460, 11778, or 14484 Leber's Hereditary Optic Neuropathy Mitochondrial DNA Mutation
  Journal of Biological Chemistry, 2000
• PERK mediates cell-cycle exit during the mammalian unfolded protein response
  Proceedings of the National Academy of Sciences, 2000
• Mammalian unfolded protein response inhibits cyclin D1 translation and cell-cycle progression
  Proceedings of the National Academy of Sciences, 1999
• Retrograde Ca2+ signaling in C2C12 skeletal myocytes in response to mitochondrial genetic and metabolic stress: a novel mode of inter-organelle crosstalk
  The EMBO Journal, 1999